Applied nutritional investigationNicotine may affect the secretion of adipokines leptin, resistin, and visfatin through activation of KATP channel

- Serum leptin, resistin, and visfatin were significantly upregulated in male smokers.
- Nicotine treatment increased leptin, resistin, and visfatin secretion in 3T3-L1 adipocytes.
- The resistin and visfatin secretion was reduced by KATP channel inhibitor, but leptin secretion was not changed.
- Nicotine might influence secretion of adipokines through KATP channel.

ObjectiveIt has been confirmed that adipokines are associated with atherosclerosis. Cigarette smoking was found to possibly influence adipokine secretion. However, the precise role of smoking in adipokine secretion and the underlying mechanisms are largely unknown. The aim of this study was to determine whether nicotine, the principal active ingredient of cigarettes, can influence adipokine secretion and its potential mechanism.MethodsThe present study consecutively enrolled 96 men, including 50 smokers with early atherosclerosis and 46 nonsmokers. Serum adipokines, including leptin, resistin, and visfatin, were determined with enzyme-linked immunosorbent assay in all participants. Furthermore, the effect of nicotine on secretion of these adipokines was examined in differentiated 3T3-L1 preadipocytes under the conditions of ATP-dependent potassium (KATP) channel blocked or unblocked.ResultsCompared with the control group, serum levels of leptin, resistin, and visfatin in smokers were significantly higher. In 3T3-L1 adipocytes, nicotine treatment significantly increased the levels of these adipokines (P = 0.014, 0.001, and 0.029, respectively). When the KATP channel was blocked, secretion of resistin and visfatin was reduced (P < 0.001), but no change was found in the leptin secretion (P = 0.522).ConclusionsNicotine may affect the secretion of adipokines leptin, resistin, and visfatin through activation of KATP channel.